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2005 | 52 | 4 | 897-902
Article title

The effect of Topotecan on oxidative stress in MCF-7 human breast cancer cell line

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Abstracts
EN
Purpose. Topotecan, a semisynthetic water-soluble derivative of camptothecin exerts its cytotoxic effect by inhibiting topoisomerase I and causes double-strand DNA breaks which inhibit DNA function and ultimately lead to cell death. In previous studies it was shown that camptothecin causes ROS formation. The aim of this study was to investigate if Topotecan like camptotecin causes oxidative stress in MCF-7 human breast cancer cell line. Determining the oxidant effect of Topotecan may elucidate a possible alternative mechanism for its cytotoxicity. Experimental design. MCF-7 cells were cultured and exposed to Topotecan for 24 h at 37°C. The viability of the cells (% of control) was measured using the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Lipid peroxidation (TBARS), protein oxidation (carbonyl content), sulfhydryl, glutathione (GSH) levels, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities were determined in MCF-7 cells with and without Topotecan incubation. Results. We found the IC50 concentration of Topotecan as 0.218 µM in MCF-7 cells. This concentration of Topotecan was used in the incubations of the cells. Our data indicated increased oxidative status, as revealed by increased lipid peroxidation and protein oxidation, and decreased GSH and sulfhydryl levels in MCF-7 cells exposed to Topotecan compared to control cells. In contrast, there was a slight increase in SOD and a significant increase in GPx and catalase activity in MCF-7 cells incubated with Topotecan compared to the control. Conclusions. These results support our hypothesis that Topotecan increases oxidative stress in MCF-7 cells.
Year
Volume
52
Issue
4
Pages
897-902
Physical description
Dates
published
2005
received
2005-02-10
revised
2005-06-23
accepted
2005-06-30
(unknown)
2005-11-07
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Document Type
Publication order reference
YADDA identifier
bwmeta1.element.bwnjournal-article-abpv52p897kz
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